Abstract

Helicobacter pylori is a Gram-negative bacterium which chronically infects the stomach of > 50% of the human population and is the major cause of gastro duodenal pathologies ranging from peptic ulcers to gastric cancer. There is a strong inflammatory component to these diseases and H. pylori gastric colonization is typically accompanied by mucosal infiltration of neutrophils, macrophages and Th1 lymphocytes, with a production of IL-12 and IFN-γ. However, an inverse association between the H. pylori infection and asthma has been also recently reported. Bronchial asthma is characterized by Th2 inflammation, which is inhibited by IL-12 and IFN-γ. A number of studies demonstrated that in allergic asthmatic patients, the Th2 responses can be redirected toward Th1 by H. pylori, specifically through the activities of its protein HP-NAP. Moreover, administration of HP-NAP limits the accumulation of eosinophils in the lung and prevents an increase of serum IgE in a mouse model of allergic asthma. These results could provide a possible biological function for HP-NAP and might be a part of the molecular mechanism underlying the inverse association between H. pylori infection and asthma.

Key words: Cytokines, Helicobacter pylori, asthma, HP-NAP